SA4503, a sigma-1 receptor agonist, prevents cultured cortical neurons from oxidative stress-induced cell death via suppression of MAPK pathway activation and glutamate receptor expression

@article{Tuerxun2010SA4503AS,
  title={SA4503, a sigma-1 receptor agonist, prevents cultured cortical neurons from oxidative stress-induced cell death via suppression of MAPK pathway activation and glutamate receptor expression},
  author={Tuerhong Tuerxun and Tadahiro Numakawa and Naoki Adachi and Emi Kumamaru and Hiromi Kitazawa and Motoshige Kudo and Hiroshi Kunugi},
  journal={Neuroscience Letters},
  year={2010},
  volume={469},
  pages={303-308}
}
Sigma receptor ligand, (+)-pentazocine, suppresses inflammatory responses of retinal microglia.
TLDR
Treatment with (+)-pentazocine suppressed inflammatory responses of retinal microglia and inhibited LPS-induced activation of ERK/JNK MAPK and may exert neuroprotective effects through manipulation ofmicroglia in neurodegenerative disease.
Sigma 1 receptor regulates ERK activation and promotes survival of optic nerve head astrocytes
TLDR
Treatment of ONHAs with (+)-pentazocine attenuated the level and duration of stress-induced ERK phosphorylation following oxidative stress exposure and promoted survival of OnHAs, suggesting that S1R activation suppresses ERK1/2 phosphorylated and protects ONH as from oxidative stress- induced death.
Sigma-1 Receptors and Neurodegenerative Diseases: Towards a Hypothesis of Sigma-1 Receptors as Amplifiers of Neurodegeneration and Neuroprotection.
TLDR
It is suggested that sigma-1 receptor dysfunction worsens disease progression, whereas enhancement amplifies pre-existing functional mechanisms of neuroprotection and/or restoration to slow disease progression and suggest future clinical applications of s Sigma-1 ligands as part of multi-therapy approaches to treat neurodegenerative diseases.
Sigma-1 Receptor: A Potential Therapeutic Target for Traumatic Brain Injury
TLDR
This review summarizes the current knowledge of the Sig-1R, its mechanistic role in various pathophysiological processes of multiple CNS diseases, and its potential therapeutic role in TBI.
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